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Übersetzung für 'Íkr' von Englisch nach Deutsch

Icelandic krona <ISK, kr, Íkr>

Isländische Krone {f} <ISK, kr, Íkr>curr.

• Isländische Krone {f} <ISK, kr, Íkr> = Icelandic krona <ISK, kr, Íkr>

• However, it also blocks IKr (Kv11.1) channels (see hERG gene) so can pose a risk for torsades de pointes. This cardiotoxicity is concentration dependent.
• KCNE1 also regulates hERG, which is the Kv α subunit that generates ventricular IKr. KCNE1 doubled hERG current when the two were expressed in mammalian cells, although the mechanism for this remains unknown.
• Vanoxerine is a piperazine derivative which is a potent and selective dopamine reuptake inhibitor (DRI). Vanoxerine binds to the target site on the dopamine transporter (DAT) ~ 50 times more strongly than cocaine, but simultaneously inhibits the release of dopamine. This combined effect only slightly elevates dopamine levels, giving vanoxerine only mild stimulant effects. Vanoxerine has also been observed to be a potent blocker of the IKr (hERG) channel.
• The action of azimilide is directed to the different currents present in atrial and ventricular cardiac myocytes. It principally blocks IKr, and IKs, with much weaker effects on INa, ICa, INCX and IK.Ach. The IKr(rapid)and IKs (slow) are inward rectifier potassium currents, responsible for repolarizing cardiac myocytes towards the end of the cardiac action potential. A somewhat higher concentration of azimilide is needed to block the IKs current. Both blockages result in an increase of the QT interval and a prolongation of atrial and ventricular refractory periods.
• In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca2+ and the opening of the rapid delayed rectifier potassium channels (IKr).

• Quinidine also blocks the slowly inactivating, tetrodotoxin-sensitive Na current, the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito.
• Dofetilide works by selectively blocking the rapid component of the delayed rectifier outward potassium current (IKr).
• AF and TdP may be induced with L-type calcium channel hyperactivity and increased calcium release from the sarcoplasmic reticulum. The L-type calcium current is also blocked by AZD 1305 which suppresses the intracellular rises in calcium levels and calcium oscillations that produce EADs. The combined block of INa, IKr, and L-type calcium current is key to the anti-arrhythmic potential of AZD1305 compared IKr blockade alone.
• Most anti-arrhythmic medications exert their effects by decreasing the permeability of potassium ion channels (IKr) in heart cells. These potassium channel blockers delay ventricular repolarization and prolong action potential duration (APD; the prolongation of the electrical stimulus within heart cells). These changes can lower heart rate, eliminate atrial fibrillation, and ultimately sudden cardiac death. HBI-3000 suppresses early afterdepolarizations (EADs; a change in the normal net flow of ions during repolarization), does not produce any electrical abnormalities, and displays minimally pronounced prolongation of APD during a slow heart rate (i.e. stimulated at a slower frequency). Pronounced prolongation of APD during a slow heart rate can lead to proarrythmias. Overall, HBI-3000 seems to have a low proarrhythmic risk. The effect of HBI-3000 on contractility and cardiac conduction requires further investigation.